Abstract

Compelling evidence suggests that alteration of normal prenatal development influences one's lifetime risks for obesity and cardiovascular disorders, which are components of the metabolic syndrome. Reflecting the public health importance of elucidating risk factors for obesity and cardiovascular disease, the metabolic syndrome affects nearly 50 million Americans. Thus, efforts aimed at elucidating the risk factors for adult disease, including those that contribute to a small element of causation, are of major public health and economic importance. The goals of this proposal are to identify the mechanisms by which adenosine acts to protect the embryo in utero and how altered embryonic adenosine action leads to long-term adverse effects in adulthood.

  Funding Agency

Agency
National Institute of Health (NIH)
Institute
Eunice Kennedy Shriver National Institute of Child Health & Human Development (NICHD)
Type
Research Project (R01)
Project #
5R01HD058086-02
Application #
7938832
Study Section
Pregnancy and Neonatology Study Section (PN)
Program Officer
Ilekis, John V
Project Start
2009-09-30
Project End
2012-08-31
Budget Start
2010-09-01
Budget End
2012-08-31
Support Year
2
Fiscal Year
2010
Total Cost
$410,198
Indirect Cost

  Institution

Name
Yale University
Department
Pediatrics
Type
Schools of Medicine
DUNS #
043207562
City
New Haven
State
CT
Country
United States
Zip Code
06520

  Publications

Rivkees, Scott A; Wendler, Christopher C (2017) Long-term consequences of disrupting adenosine signaling during embryonic development. Mol Aspects Med 55:110-117
Fang, Xiefan; Poulsen, Ryan R; Wang-Hu, John et al. (2016) Knockdown of DNA methyltransferase 3a alters gene expression and inhibits function of embryonic cardiomyocytes. FASEB J 30:3238-55
Fang, Xiefan; Poulsen, Ryan R; Rivkees, Scott A et al. (2016) In Utero Caffeine Exposure Induces Transgenerational Effects on the Adult Heart. Sci Rep 6:34106
Fang, Xiefan; Robinson, Jourdon; Wang-Hu, John et al. (2015) cAMP induces hypertrophy and alters DNA methylation in HL-1 cardiomyocytes. Am J Physiol Cell Physiol 309:C425-36
Fang, Xiefan; Mei, Wenbin; Barbazuk, William B et al. (2014) Caffeine exposure alters cardiac gene expression in embryonic cardiomyocytes. Am J Physiol Regul Integr Comp Physiol 307:R1471-87
Buscariollo, Daniela L; Fang, Xiefan; Greenwood, Victoria et al. (2014) Embryonic caffeine exposure acts via A1 adenosine receptors to alter adult cardiac function and DNA methylation in mice. PLoS One 9:e87547
Rivkees, Scott A; Wendler, Christopher C (2012) Regulation of cardiovascular development by adenosine and adenosine-mediated embryo protection. Arterioscler Thromb Vasc Biol 32:851-5
Buscariollo, Daniela L; Breuer, Gregory A; Wendler, Christopher C et al. (2011) Caffeine acts via A1 adenosine receptors to disrupt embryonic cardiac function. PLoS One 6:e28296
Poulsen, Ryan R; McClaskey, Carolyn M; Rivkees, Scott A et al. (2011) The Sphingosine-1-phospate receptor 1 mediates S1P action during cardiac development. BMC Dev Biol 11:37
Rivkees, Scott A; Wendler, Christopher C (2011) Adverse and protective influences of adenosine on the newborn and embryo: implications for preterm white matter injury and embryo protection. Pediatr Res 69:271-8

Showing the most recent 10 out of 11 publications